Saturday 21 April 2012

HOW YOUR BODY KEEPS YOU WELL

How Your Body Keeps You Well
By RUTH and DEWARD BRECHER
“Not sickness but health,” a famous physician once remarked, “is the greatest of medical mysteries.”
Your own good health is an example.  Every day your body is assailed by millions of germs, many of which can produce illness or even death.  Yet you stay well.  Countless bacteria and viruses gain entry into your body with the food you eat or the air you breathe or through breaks in your skin.  Yet you stay well.  Some of them establish permanent residence in your mouth, your nose and throat, or your intestines, where they may multiply fantastically.  Yet you stay well.
What protects you from these ceaseless assaults by bacteria and viruses?
Though decades of study scientists have been slowly finding out.  Your health is safeguarded, they report, by an ingenious series of defenses arranged in depth like the successive lines of an army entrenched to ward off invaders.
Suppose, for example, that a germ-laden fleck of dust floats into your eye.  In all probability there is nothing to worry about.  Your eye surface is constantly bathed in tears, which contains a bacteria-destroying antiseptic called lysozome.  Lysozome is so powerful tat a single teardrop diluted with half a gallon of water will still destroy at least one species of germs.
Your saliva and other fluids manufactured by your body also contain lysozome, as well as other antiseptic chemicals called leukins, lysine and plains, which have not yet been fully studied.  Even your bare skin has considerable germicidal power.  For example, virulent dysentery bacteria in a drop of fluid placed on a glass slide will survive for hours, while those in a drop placed on the clean palm of your hand will be dead within about 20 minutes.
Some kinds of germs can survive these external defenses and even multiply on your skin.  Before they can harm you, however, they must gain entry into your body and then run an amazing gantlet of other defenses.  Antiseptics in your saliva, for instance, attack germs entering through your mouth.  For those that are swallowed and washed into your stomach powerful digestive juices lie in wait.  Few of the harmful bacteria reach your intestines alive.
Germs that gain entry through your nose must thread the complicated maze of your air-filtering nasal passages.  The surfaces of these passages are kept moist by mucous fluid that acts like flypaper in catching germs. If the germs cause irritation, they are sneezed out; or your nose starts to run and they are flushed out.  Germs that manage to reach the tubes to the lungs are also trapped in a mucous fluid, and are sometimes coughed out.  Tiny hairs like fibrils are constantly waving in the mucous fluid, propelling it toward your throat.  Germs trapped in the fluid and meet their fate in the well-guarded gastrointestsstinal tract.
When germs get into your body through breaks in your skin or mucous surfaces—breaks so small that they may be unnoticed—the peril is seemingly greater.  Let’s say that you step on a germ-laden nail.  Watch germ thus entering your tissues may divide into two after 20 minutes.  If this rate were to continue, you would be host to a million descendents within seven hours, and they and to several quadrillion next day.  By then your entire body would, of course, be overwhelmed.  But before this can happen another type of defense, called inflammation, will have come to your aid.
Inflammation begins when various chemicals are released at the site of a germ invasion by the invaders or by the injured cells in your body.  These chemicals seep outward in all directions until they reach the nearest blood vessels.  There they cause a relaxing of the vessel walls that enables plasma, the watery part of the blood, to seep out.  Accompanying the blood plasma are white cells called leucocytes, and various chemicals that curb bacterial growth.
Leucocytes are among the most curious and most effective of your body’s defenses.  In appearance they resemble the one-celled animal called amoeba, and like the amoeba they can propel themselves from place to place within your body.  In some way most yet understood leucocytes are attracted as if by a magnet to the site of a bacterial invasion.  When they arrive they gobble up any invading particles they find.
It is fascinating to watch this gobbling-up process through a microscope.  A leukocyte slithers up an invading bacterium, crowds it against a solid surface, then flows its jelly-like body around the bacterium to “corner” it.  Next it opens a b\hole in its skin-like membrane, and the bacterium is completely engulfed.  A moment later the leukocyte slithers off after its next quarry.  Millions of leucocytes are often mobilized at the site of an infection.
Other factors involved in inflammation help the leucocytes in their work.  In blood plasma is a chemical called fibrinogen (the chemical responsible for blood clots), which quickly solidifies into a network of strands and, with other plasma substances and the leucocytes, forms a wall around the battlefield, trapping the germs so that the infection is localized.  Boils and abscesses are typical examples of how this walling-off process safeguards the rest of your body from germ invaders.
Even though bacteria are thus contained, the resources of your entire body are mobilized to defeat them.  Some of the chemicals released during the battle enter your blood stream and carry the alarm to storehouses throughout your body where leucocytes reserves and maintained.  Within minutes millions of additional leucocytes are released into your blood, which carries them to all your tissues.  While this is going on, your bone marrow is also alerted and it speeds up the manufacture of new leukocyte reserves.
Some germs are coated with a repellent, which keeps leucocytes away, and some have the power to kill the leucocytes that engulf them.  Even in death, however, the leucocytes continue to release chemical injurious to germs.
If the leucocytes cannot complete the mopping-up operation, they are joined by larger (but still microscopic) cells called macrophages.  These can gobble up not only bacteria but also leucocytes that are harboring bacteria.
Usually when leukocyte or macrophage engulfs a germ it means death to the germ, but not always.  Some bacteria can survive for long periods within cells which have gobbled them up, indeed, a cell may occasionally prolong the life of a bacterium by protecting it from antiseptic blood substances and from the drugs your physician prescribes to help combat the infection.  Your body requires a way to dispose of these germs after they have been engulfed, and of other waste products.
To provide for this, a network of channels called the lymphatic system drains your body tissues.  Leucocytes, macrophages and invading particles enter the vessels of this network and are carried by the lymph fluid to “regional lymph nodes,” the glands, situated at strategic points through your body.  Each node serves as a filter, holding back bacteria and other particles.  The lymph fluid flows on from one node to another until it reaches the ones in the neck, where it is discharged into the blood stream.  By then, generally, all germs have been filtered out of the lymph fluid.
Following an illness, however, disease germs may survive for days or even weeks within the lymph nodes.  The glands in your neck are the final barriers, which prevent germs from reaching your blood stream, and the survival of germs in them for long periods explains shy these glands sometimes remain swollen and tender long after other symptoms have disappeared.
Even if a few germs reach the blood stream, another alien of defense stands ready.  Your bone marrow, liver, spleen and a few smaller organs are equipped with multitudes of macrophages to filter invading particles out of your blood just as the lymph nodes filter your lymph fluid.
How ate these leucocytes and macrophages able to distinguish between invading germs or other particles and the cells or molecules of your own body?  Your body has a built-in identification system, which labels invading particles!  These labels, which attach themselves to invaders, are called antibodies.  Leucocytes and macrophages will occasionally engulf almost any particle they happen upon, but the ones they search out and devour with the greatest voracity are those, which have been labeled as invaders by antibodies.
Most cases of recovery from an infection are traceable in large part to antibody action.  If you have ever had scarlet fever, your body lacks antibodies tailored to fit the streptococci, which cause these diseases.  But if streptococci secure a sufficient toehold in your body to multiply, your antibody factories start tooling up.  For several days, perhaps, the germs continue to multiply and you get sicker and sicker.  By then, however, full-scale antibody production has begun and antibodies are turned out in large amounts.  These latches into the scarlet-fever streptococci, which as soon as they are libellee, fall prey to the voracious leucocytes and macrophages, and your recovery begins.  Substances in your blood called complement also help out by destroying bacteria to which antibodies are attached.
It is chiefly your antibodies, which make you immune to second attacks of many common illnesses.  The first time you suffer from a disease such as scarlet fever or measles your antibody factories take several days to learn the right pattern.  Once the lesson is learned, however, production can begin much more promptly, and large amounts of antibodies of the desired pattern may be turned out within a few hours after the entry of a few thousand germs.  Thus the second and subsequent invasions of a particular type of germ are frequently wiped out before you even suspect that you’ve been infected.
Antibodies are also the agents, which make in possible to control infectious diseases through vaccination.  A vaccine is a substance, which teaches your body in advance how to manufacture antibodies promptly against a disease you have not yet encountered.  The Salk Polio vaccine, for instance, uses polioviruses, which have been killed by formaldehyde to teach your body how to manufacture antibodies against living polioviruses.
A few kinds of germs have learned how to evade our antibody defenses.  The influenza virus is the most striking example.  Every few years a type of flu virus comes along which is unaffected by common flu antibodies.  When this happens, influenza “pandemic” sweeps the world.  Witching a few years almost everybody gets the new kind of flu and develops antibodies against it—and about this time a new strain of the flu viruses pops up.  Each type of flu requires a separate antibody.
Most of the antibodies circulating in your blood are found in a part of the blood plasma called gamma globulin.  This antibody-rich substance ca be extracted from the blood of donors and stored for considerable periods.  Small injections of gamma globulin will provide temporally immunity to measles and infectious hepatitis; the “borrowed antibodies” in the gamma globulin act just like the antibodies you manufacture yourself.
Newborn babies also stay well on borrowed antibodies.  Their antibody factories operate poorly or not at all during the first few weeks of life, but antibodies received from their mothers before birth protects them for a time from most of the diseases to which the mothers themselves are immune.  Babies also get protective antibodies in mother’s milk, especially in the milk secreted during the first few days of nursing.
Some germs attack only cells in their immediate vicinity; others release poisonous molecules called toxins which may circulate to other parts of the body.  Diphtheria and tetanus bacteria are examples of these toxin producers.  When attacked by toxins your body manufactures antitoxins—that is, antibodies against toxin molecules.  And just as you can be immunized against virus diseases by means of vaccines containing denatured viruses, so you can be injections of denatured toxins called toxics.
Could mankind survive without the human body’s miraculously coordinated “defense in depth?  It seems unlikely.

IT WON'T HURT, CAUSE YOU'RE MY BROTHER

It Won’t Hurt, Cause You’re My Brother”
By NILAH RODGERS

Football was the most important thing in 14-year-old Todd Conner’s life, until his brother Allen was born, on October 7, 1975.  The squirmy nine-pound infant charmed the would-be grid star, and soon Tood was vying with his sister Lori Ann, 15, for opportunities to help their mother with the new arrival.

One afternoon in November—less than six weeks after the baby’s birth—Todd was holding Allen in the crook of his arm, natural as football.  As he lowered the baby into the bassinet, he noticed that the infant’s head was wet with perspiration.  Todd held out a finger and five tiny fingers twined around it.  Then, suddenly, the chubby hand tightened convulsively and the baby’s body went limp.

“Mother!” Todd shouted.  “Something’s wrong!”

Unable to revive, her infant son, Carolyn Conner rushed Allen 20 miles from their home in Conyers, Georgia, to Henrietta Engleston Hospital for Children in Atlanta.  Their doctors shaved off his blond ringlets and punctured the soft spot on his head with intravenous needles attached to tubes.  Physicians probed, palpated and X-rayed; technicians pricked the tin fingers, drawing blood, and left with pipettes filled, slides carefully smeared and labeled.  Nurses collected urine samples recorded his fluid intake, blood pressure and temperature.
Two days later, the diagnosis showed that Allen had suffered permanent kidney impairment.  The two vesico-ureteral valves on the tubes leading from the kidneys to the bladder did not function properly.  Thus, urine flowed back into his kidneys, severely damaging them.

To repair the valves and stop the backup, Allen needed surgery.  But he was too young and weak for such an intricate operation.  Instead, the surgeons opened Allen’s abdomen and made an incision in his bladder to excess urine could drain through a catheter.  The major surgery would have to wait until he weighed at least 16 pounds.

The first time he saw his baby brother with the needles inserted into the veins beneath his scalp, Todd turned away.  “Does it hurt him? He asked weakly.  Though his father, Perry Conner, and his mother and the nurses assured him Allen couldn’t feel the needles, Todd’s own head hurt sympathy.

Seven weeks after entering the hospital, Allen was allowed to go home.  The interim surgery had put life back to him.  He learned to sit up and crawl.  However, at seven months, he still weighed less than his birth weight.

One day Tood found him asleep in the family room and saw that his skin was white as talcum powder.  Todd’s yell immediately brought his mother.  She grasped the skin of the baby’s abdomen between her thumb and forefinger.  Instead of being supple and falling back in place, the pinched-up ridge remained.  “He’s dehydrated,” Carolyn said, gathering Allen up and heading for the hospital.
This time it was five weeks before doctors let the boy come home, and after they did there was a family council.  “The nephrologist says Allen will probably develop kidney failure-possibly before he’s a year old,” Carolyn explained, her voice shaking.
But during the following weeks, with diet and heavy meditation, Allen’s condition stabilized.  His birthday came and went: Tood organized a party for him, with cake, punch and balloons.  He learned to walk, stand on his head, whistle, and pull off his clothes.  His favorite pastime was galloping around the house on Todd’s back, shouting, “Go, horsy!”
By December 15, 1976, Allen weighs 16 pounds and the Atlanta nephrologist told Carolyn Conner that he could now withstand the valve-reimplantation surgery.
Allen knew from his earlier hospitalizations that “losing” his shoes, meant pain would follow.  When his parents had their tiny son ready for the hospital, Todd bent down and tied a double knot in his brother’s shoelaces.  “Hang on to these shoes, boy,” he said with affection.  Then prayed: ‘Dear God, please let him come back.’
The operation went smooth and Allen returned home on Christmas Eve, weighing 13 pounds.  His favorite Christmas toy came from Todd—a big green frog he could ride, even when he felt so bad he couldn’t walk.  Once again the toddler commandeered Todd for his horse and made him his general slave.
Allen’s well being lasted until July 1977.  Then he lost his appetite.  Nothing, not even Todd’s coaxing, could get him to eat enough to maintain his weight.
Doctors suggested garage—force-feeding through a tube inserted in Allen’s nose and running into his stomach.  With a high-calorie formula and four daily feedings, the boy gained a little weight and grew an inch.  Meanwhile, his blood tests, taken every other day, indicated stable kidney function.
Then suddenly in January 1978, the tests showed further deterioration.  By mid-January he walked unsteadily he walked unsteadily, and by mid-February he stumbled occasionally.  Again the Conners took him to a specialist in Atlanta.  The doctor said he had a bone disease that goes with kidney failure.
By March, Allen could hardly walk.  So Todd carried him the burden of his knowledge far heavier than his little brother.  Every time the child was taken to the doctor, Todd insisted on a complete report.  Twenty-five times Allen’s head had been shaved for intravenous feeding.
Now came new word from the specialist: Allen must go to the University of Minnesota Hospital for hemodialisis, a blood cleaning process—called dialysis for short.
“The hospital is world-famous for its success in treating kidney diseases in very young children,” Carolyn Conner assured her family.  Then after a long pause she added, “Allen will have to have a kidney transplant this summer.  If it’s successful it will cure the bone disease too.”
For a moment Todd could not speak.  Then he lifted his eyes to his parents.  “Mine,” he said.  “I want to give Allen one of my kidneys.”
“Todd, your mom and I thought you’d volunteer,” his father replied.  “But we’re against it.  If either you or Lori give a kidney and it didn’t work, and then something happened to you…” He chocked over the words.  “Besides, with only one kidney, you might not be able to play football.”
“I don’t care about that!” Todd blurted.  “Allen needs a kidney, and when that plane leaves Minneapolis, I want to be on it with him.  You’ve got to let me be tested.”
One week later, Todd and Lori Ann—who had also countered a kidney and insisted on being tested—sat with their parents in the office of Dr. John Najarian at the University of Minnesota Hospital.  “Rejection is the major concern,” Najarian said, ‘so we check for tissue compatibility.  Tissue typing is done through four genetic makers called antigens.  For a donor and recipient to be compactable, at least two antigens must match from a sibling, there’s a 90 to 95 percent change of success.  It’s a 70 to 75 percent chance if the donor is a parent, and 50-50 if it’s some other family member.”
Perry and Carolyn Conner, and Lori, all proved two antigen matches.  Todd showed a four-antigen match—so close to Allen’s tissue that only an identical twin could be more compactable.  His parents consented to the transplant.
While 2 ½ -year-old Allen continued dialysis as an outpatient, Todd began the psychological testing required before such surgery.  One day the topic was sports.  The psychologist asked, “You think you’re a pretty good football player?”
“Fair,” Todd muttered.
“Ever dream of being the fasted back, the highest-scoring end?”
“Yeah, I’ve thought about it.”  Todd’s voice was high, tense.
When the session was over, Todd dent to the dialysis section of the hospital and stood outside the door listening to the soft whir of the machines cleaning his brother’s blood—a four-hour, three-times-a-week process.  He scuffed his toe, the way he’d do for an onside kick.  How did that doctor guess about those dreams”?  Yes, he would miss sports, especially football.  But he’d have something better to take its place: the finest little brother who ever lived.
On May 10, 1978, Todd woke early, long before the scheduled 6:30 a.m. surgery.  Despite the pills meant to calm him, butterflies churned in his stomach the way they did before a big game.  A hospital orderly bumped opens his door with rolling bed.  The 16-year-old climbed abroad and was wheeled off toward surgery.
“Todd!”  He heard his brother’s voice, shaky with tears.  An attendant pushed another cart toward him with a tiny lump under the sheet—Allen.  The little boy looked white and afraid, but his right arm wiggled out from under the sheet, and he waved and smiled.
The orderlies pushed the carts into the same elevator.  Allen kicked his sheet off, exposing red shakers—laced and tied in a double knot!  He climbed over on Todd’s cart and locked his skinny arms around his brother’s neck.
“After today,” Todd said huskily, “you’re not going to hurt anymore.”
“ Know,” said Allen.  Suddenly his chin began to quiver.  “Todd, when they give me part of you, will you hurt?”
Hiss little brother had suffered so much, yet here he was worrying about him.  “Nope,” Todd said, pulling Allen close.  “It won’t hurt me, because you’re my brother.”
The elevator door slid open and the attendants rolled them toward adjoining rooms.
A dozen green-clad doctors and nurses clustered around Allen.  An incision was made down the middle of his abdomen, and his shriveled kidneys were removed.  Then Dr. Najarian went into next room where another surgical team had opened Todd halfway around at the waist on one side, to remove the right kidney.  Dr. Najarian returned almost immediately, cupping in his big hands something that looked like a shiny wet potato.  He placed it in a basin of sterile solution to wash away the blood and cool the kidney for a better take.  Meanwhile, Todd’s incision was closed and he was whisked to recovery.
Allen’s abdominal cavity looked far too small to accept his brother’s kidney, nearly three times the size of his own.  It was a tight fit, but doctors knew that soon after the operation the kidney would shrink to the size Allen needed.  Then, as he started to grow, it would grow with him at a normal rate.  Six hours elapsed before Dr. Najarian, grinning with relief, reported to the Conners that Todd’s kidney was functioning in Allen.
The next day Todd asked to be wheeled down to Allen’s room.  Through the bed railing the two brothers kissed and repeated each other’s names over.  For the next two weeks, Allen received interjection serum—administered via tube inserted in his neck during surgery.  Then, 14 days after surgery, Allen and his parents flew home to Georgia. [Todd had left a week later].
Today, nearly three years later, with his doctor’s approval, Todd is working as a landscaper in his father’s business.  Allen is in kindergarten and has achieved the normal height and weight for a child of his age.  Once a month his mother takes him for blood tests at a nearby clinic; the results are phoned to Minnesota for monitoring.  For the rest of his life he will take ante rejection medication.  But thanks to Todd’s precious gift, the lively 5-year-old now has a future, a chance for a full and happy life.

Friday 20 April 2012

I'VE LIVED WITH CANCER


I’ve Lived With Cancer
By VIRGINIA HILTON WHITNEY: as told to WATTER S. ROSS
One morning I stretched in bed and felt a pain in my right breast.  I touched the spot with my fingers; there was a tiny lump, about half the size of an olive.  I lay there for a minute thinking.  I was 37 years old.  What a terrifying coincidence.  Mother had been 37 when she had her operation for breast cancer.  I wasn’t sure my lump was anything serious, but I remembered how it had been with Mother.  She was the sort of person who believed it a disgrace to be ill.  She waited too long to see the doctor.  Ger operation hadn’t cured her; the cancer recurred in the uterus, and the second time they didn’t operate.  They treated her with radium, but that didn’t work either.  She died when I was 19, a senior in college.
With these memories crowding in one me, I wanted to see a doctor right away.  My husband Hod (a nickname for Horace) and I, with our two little girls, had just moved to Seattle, and we didn’t know any doctors there.  After a bad experience with obstetrician who diagnosed the lump as “just nerves,” I went eventually to an internist.  He felt the lump and send me immediately to a surgeon.  The surgeon told me the lump ought to come out the next day.  He would have it examined on the spot by a pathologist.  If it turned out to be cancer, he would go right ahead and do a radical mastectomy; remove the breast and all surroundings tissue likely to be invaded by cancer, including some muscles and the lymph nodes under the arm.  He knew about my mother and wasn’t about to take any chances.  I was pretty sure it wasn’t cancer.  I may have prayed about it.  Raised a Presbyterian, I had married a Mormon.  Not wanting a house divided, my daughter and I had studied Mormon faith and been baptized the preceding year.
I knew the bible quotation: “Is any sick among you? The prayer of faith shall save the sick,” we asked some of out Mormon friends, elders in the church, to come to the hospital and pray.  They came, put their hands on my head and asked the Lord’s blessing, and prayed for my recovery.  It was a simple, spontaneous act, not words read out of a book.  But in this time-honored ceremony.  I knew I had been blessed—that there had been communication with Our Lord.
The next day, when I was taken to the operating room, both Hod and I were quite calm.  When they didn’t bring me out after a few hours, he knew that they must have found cancer.  He says he didn’t worry, and I believe him.  He has a calm faith in God, and he trusted our doctors—and he has always made me feel the same way.
My friend thought when I woke up after the operation was that there was a ten-ton truck on my chest.  This was the pressure bandage put on to keep fluid from accumulating.  “We’re sorry,’ a doctor said, “but we had to do the radical.”  I was pretty groggy from the anesthesia, but even so I was shocked.  Remember, I was only 37—that seems very young to me now, 16 years later—and I was proud of my body.  I knew what the alternative was, though, and the doctors cheered me by saying that they had got out all the cancer in one piece of tissue.  As far as the surgeons could tell, I was free of disease: “You might as well worry about being hit by an automobile,” he said.  “As to think that you will die of cancer.”
But what really convinced me that I was going to live was a peculiar experience I had a day or two after the operation.  I was lying in bed, quite alone, when I heard a voice say, “You are going to be fine.”  It’s possible that I was still feeling the effects of drugs, but I heard that voice as clearly as I’ve ever heard anything in my life.  It dramatically renewed my faith, gave me strength and tranquility.
After nine days I was able to go home.  Hod came and got me.  He acted as though I had just got over a bad cold, or something equally trivial.  That night we watched a television verity shoe with a line of chorus girls wearing low-cut gowns.  I began to cry.  Hod turned to me and said, “and what are you crying about?”  It made so mad that I quiet crying—and I’ve never cried since.  What he said may seem heartless, but he was under doctor’s orders: tender, loving care was great, but sympathy would only get me feeling sorry for myself.
I was very touchy at first.  The doctor said, “You must have something to help you bathe; otherwise you might lose your balance and fall.”  When I protested, “You don’t mean you want me to let my husband see me!” he just laughed and said, “Of course I do.”  And Hod was so unconcerned about the scar that I began to get over my embarrassment.  About four weeks after the operation, I went to a department store for my prosthesis—a false breast worn in a brassiere.  The woman in the lingerie section was merry understanding, and the prosthesis was quite comfortable.
After a radical mastectomy you have to work to recover the use of your arm.  It is painful, because the muscles have been cut; but if you don’t exercise they heal in a stiff and awkward way.  So I did what the doctors ordered: walked my fingers up the wall, waved my arms, everything to get the motion back.  I love golf, and was especially anxious to get back to it.  There were some twinges as I began swinging a club, but I kept at it.  When I first went out to the course, I was rather nervous.  But I took a full swing and something tense me relaxed as that white ball flew into the sun.  It was a nice drive, straight done the fairway.
I was even more nervous the first time I put on a bathing suit at a friend’s pool.  Would my scar, which went rather high in my neck, embarrass the others?  Well, nothing risked, nothing gained.  It was hot, and I wanted to swim.  So I walked out, trembling a little inside, and dived into the pool.  Nobody even noticed.
As the years passed, the operation receded from by thoughts.  The girls grew up and married.  Hod and I had a wonderful time.  Of course I had the checkups the doctors ordered, including chest X-rays and the Pap test, every six months at first and then every year.  But there were no further problems.  I had long ago considered myself cured when I discovered a lump in my left breast as I was taking a shower.  I reported directly to my surgeon.  “I don’t know what it is.” He said, “So we’ll operate and find out.  With your history, even if the lump is not malignant, I will remove the breast.  But I’ll not do a radical unless the lump is malignant.”
Two days later they operated.  The lump was not malignant—but underneath he did find a spot of cancer.  When I came out of anesthesia, the doctor told me this—and that he had had to do the radical.  I wasn’t feeling so flippant, but my retort was, “Hurray, now I match!”  I now felt that my troubles were behind me.  The pathologist’s report was negative, meaning that the cancer had been confined to the one spot.  So I was concerned more about regaining use of the left arm as soon as possible, and seeing my new grandson, than about the threat of future disease.  Actually, the second operation was easier to take, both emotionally and physically, than the first—and I was playing golf within two months.
After moving from Seattle to Salt Lake City, I went to see dermatologist about a lingering ear infection.  He took a biopsy and told me there was local cancer-cells involvement.  “Please don’t be alarmed,” he said.  “It’s not metastasis [spreading] of the breast cancer, just a basal cell skin cancer,” But it had got into the cartilage, and needed some plastic surgery so, I entered the hospital.  As a precaution, the surgeon ordered a regular checkup, including chest X-ray, before we went to the operating room.  While I was still unconscious, he told Hod that the X-ray had disclosed a walnut-sized lump in my right lung that would have to come out.  “How are we going to tell her? He asked.  Hod said, “Just tell her.  She can stand the truth as well as I can.”
They gave me five days to recover from the ear operation, and then we went back to surgery for the lung.  It was a much longer and more difficult operation than the mastectomies, and more painful afterward.  For three days I was in intensive care.  But there was good news from my doctor.  The pathology report showed that the cancer—it was definitely metastases of the breast cancer—had been confirmed to that single tumor which he’d removed with the middle lobe of my right lung.
Nevertheless, I began to feel resentful.  I knew I’d been lucky, but I was getting a bit tired of being so lucky so many times, perhaps because I was older, 51.  But after six weeks—a month at hoe—the doctor said I was recuperating perfectly and could go with my husband to a convention in Coronado, California.  It was beautiful there, sunny and warm, and I began to feel strong again.
For a year I was fine, traveling with Hode, playing golf, visiting our grandchildren.  And them I had an attack of pneumonia.  During a series of sputum tests, cancer cells were found.  This means that there is cancer in my chest.  They’ve been giving me radiation treatments to reduce fluid accumulation, and now chemotherapy has been started.  The situation is not good, but I know that I’ve been helped before I believe my doctors when they say there is a good chance of arresting the spread of the cancer.
People often ask me if my cancer is hereditary.  The doctors say no, although they think there may be a hereditary tendency in some families for some forms of cancer.  Since my mother and I both had breast cancer, this is clear warning to my daughters, one doctor told me.  They should be extra careful as taught by the American Cancer Society.
Another question that comes up shy, after all I’ve bee through; I’m not angry or depressed.  My answer is: if the doctors give you every chance to live a normal life, well, why not does it?  They’ve always been honest with me.  They’ve said frankly in the past that they don’t know when or if another form of cancer, of another metastasis, will show up.  But I can’t see sitting around the moping.
I’ve lived a full, happy life through three major cancer operations.  I’ve watched my daughters grow up and seen three grandsons born since the first tumor.  And I’ve not been living in fear.  On the contrary, I’m more fearful about getting abroad an airplane than I am about undergoing anesthesia.  Hod and I have had a good life together; I feel we’ve had a present of 16 marvelous years—more than some have in their entire lives.  As for the future—nobly knows that except God.  And I have faith in Him, just as I have always had.

HOW WE DISCOVERED INSULIN

How We Discovered Insulin
By CHARLES H. BEST, M.D., as told to J.D.Ratcliff
The man who came into the laboratory the morning of May 16, 1921, didn’t look like a medical immortal.  Few do at age 29.  Dr. Frederick Banting looked more like a farmer—powerful, with slightly stooped shoulders, blue-green eyes, big nose and jutting, stubborn chin.  His voice, halting, quiet, betrayed an inborn shyness.
“Let’s get started, Mr. Best,” he said.  “We rally haven’t much time.”  What an understatement!  He had asked the University of Toronto for the use of a laboratory for eight weeks, for ten dogs, and for the help of someone who knew chemistry and physiology.  The money value of his modest request was $100.  With this he thought he could conquer a disease that had always baffled medical men: the merciless killer, diabetes.
“You read French, don’t you?”  Banting asked.  I did.  “Let’s to the library then.” He said, “and look up how a Frenchman named Hedon took a pancreas out of a dog.”
That was the beginning.
We both knew the horror of diabetes—described by a Greek physician 2000 years earlier as “a disease in which the flesh melts away and is siphoned off in the urine.”  Somehow the bodies of stricken people stopped burning sugar into energy.  Instead their bodies turned cannibal, consuming stored fats and proteins.  There was always unquenchable thirst—victims often drinking several gallons of water a day while losing a like amount of sugary urine.  And their appetite was ravenous.  The only treatment was a rigid diet designed for correct the patient’s disrupted chemical balance.  Severely stricken victims were offered a grim choice: eat well today ad die tomorrow, of cut down to a few hundred calories a day and linger for a white in weary befuddlement.
Banting had seen diabetes convert a cicacious 15-year-old girl classmate at Alliston, Ontario, into a pathetic child for whom death came swiftly.  At my home in West Pembroke, Maine, I had seen the same happen to my Aunt Anna.  A stout, vigorous woman in her early 30s, she wasted to 80 pounds before she died.
The world would have considered us a most unlikely pair to match wits with this killer.  I was a 22-year-old graduate student, working for my master’s degree in physiology and biochemistry.  Banting’s experience in research was virtually nil.  At his family’s urging he had started out to study for the Methodist ministry.  But, a halting speaker, he changed to medicine.  He had been an average student.
After serving as a surgeon in the Canadian army in World War 1, and winning the military Cross for bravery, he set up practice as an orthopedic surgeon in London, Ontario.  He waited for patients who never came.  One month his income was four dollars.  His fiancée could see little future with such a man, and they parted.
Noël this man was staking all his meager resources on his hunch that he could cure the sugar sickness.  He gave up his little practice, sold his office furniture, books, instruments, everything.  Banting couldn’t afford another failure.
It was known that the pancreas—a pale-yellow, pollywog shaped abdominal organ that produces digestive juices—was somehow involved in the disease.  In 1889 Oscar Minkowski in Germany had removed a dog’s pancreas, mainly to see if the animal could get along without it.  Next day he noted flies clustered around puddles of the dog’s urine.  The urine was sugary; the dog, in normal health the day before, now had diabetes.
Did pancreatic juices, then, contain a factor that normally regulated the metabolism of sugars?  To test the idea, research men tied off the ducts that carry these juices to the intestine.  When dogs got this surgery, their pancreases shriveled and generated—but they did not Ger. diabetes!  The shriveled organs, unable to send digestive secretions to the intestines, were still producing the anti-diabetic factor.
But if it wasn’t in the pancreatic juices, where was it?
Attention shifted to the thousands of mysterious little “islet” cells scattered through the pancreas and surrounded by tiny capillaries.  Did they secrete some “X” stuff, perhaps a hormone that regulated the burning of sugar?  And did they empty it, then, not into the intestine but into the blood stream?  Several research men had suggested as much and had gone hunting for the elusive hormone.  But all had come home with empty game bags.
Now it was our turn.
“Maybe it’s this way, Mr. Best.” Banting did not say—nor for several days would we become Fred and Charley.  “Maybe when the researchers remove a healthy pancreas and grind it up to extract this X stuff, enzymes in the digestive juice mix with the X stuff and destroy it—just as they break down proteins in the intestine.  Maybe that’s why no one has been able to find it.”
Knowing that when the pancreatic ducts are tied off the cells, which secrete digestive juices, degenerate faster than do the islet cells, we would tie of these ducts in dogs and wait.  “In seven to ten weeks the pancreas will degenerate, stop making digestive juices—and there will be nothing to destroy the X stuff.  You extract it.  Then we’ll give this extract to the diabetic dog and see if it lower the sugar in blood and urine.”
I did my chemical work in our cubbyhole lab.  Dog surgery was performed two flights up in the sky lighted artic.  Before summer was over, that attic became steamy as any Turkish bath.  To get some relief we wore little of nothing under our white lab coats.  Since money was short, we ate in the lab.  Eggs and sausage fried over a Bunsen burner became diet staples.
One serious problem was a scarcity of dogs.  When the situation became acute, Banting said, “Crank up the Pancreas, Charley, and let’s go.” [This was our name for hid Model T Ford.]  We rattled through the poorer parts of Toronto, hunting for dogs whose owners would part with them for a dollar.
We had tied off the first pancreatic ducts in May, and in early June we expected the pancreas to be shriveled, the X stuff accessible.  We opened one of the animals—and found the pancreas blooming with health, no atrophy, no shriveling.  Banting and I had tied the ducts incorrectly.
Our eight weeks were almost up.  But Banting was a stubborn man.  During the war he had gotten ugly shrapnel wound in hi right arm.  Doctors had wanted to amputate.  Banting refused—and nursed the arm back to health.  Now we were going to nurse our sickly project back to health.
Professor John J.R. McLeod, head of the physiology department, who had provided us with work facilities, was on vacation in Europe.  “He won’t know the difference if we way on.” We decided.
We began reporting on dogs, tying off ducts, correctly this time.  On July 27 we got the beautifully shriveled, degenerated pancreas we wanted.  It should contain the X stuff—if the X stuff existed.
Now we sliced the pancreas into a chilled motor containing Ringer’s solution and froze the mixture.  We allowed it to thaw slowly, ground it up and filtered in through paper.  A dying diabetic dog was waiting; too weak of lift his head.  Fred injected 5c.c. Of the filtrate into a vein.  The dog looked a little better—but self-diffusion is easy such times.  Blood tests were needed.
I drew a few droplets from the dog’s paw and began testing for blood sugar.  Banting hovered over me.  If sugar were heavily present the reagent in the test tube would turn deep red; little sugar and it would be a pale pink.  There was a new test every hour and the reagent was getting paler, paler.  Blood sugar was going down—form 0.20 percent, to 0.02 percent, to …  it was headed for a normal 0.09 percent!  This was the most exciting moment of Banting’s life or my own.
Life now became a blurred nightmare of work.  This thing had to be nailed down.  Dogs had to be injected, blood had to be drawn for testing, urine collected.  It was an hourly, round the-clock schedule.  We stretched out on lab benches to get what sleep we could.
But there was an ever-reviving miracle for us to behold: dogs glassy-eyed with the sleep of death upon them; then, a few hours later, they were up, tails wagging.  Jolted back to life, one dog lived 12 days, another 22 days.
Our pet was Marjorie—dog number 33.  Black-and-white, vaguely collie, she learned to jump up on a bench, hold out her paw to give us a blood sample and keep still to get the shot on which her life depended.  For 70 days she was alive, well.  Then we ran out of the extract, isletin, as we then called it. [Only later did McLeod persuade us to change the name of insulin]
It took almost all the isletin we could extract from a degenerated pancreas to keep one dog alive for one day.  How far would this to toward keeping alive millions of diabetics around the world?
Fred remembered reading that the pancreas of an unborn animal was a mainle islet cell—since the digestive juice wasn’t needed in the womb.  As a farm boy, he also knew that farmers frequently bred cows before sending them to the slaughterhouse, to hoist weight.  Wouldn’t pancreases from the unborn calves be rich in isletin?  We cranked up The Pancreas and headed for a slaughterhouse.  Later, back at the lab, we ground up the salvaged pancreas, extracted, purified and reaped a rich harvest of isletin.
We could now keep dogs alive as long as we wanted.  Eventually, of course, it was found that with improved extraction methods any animal pancreas—sheep, hog, and cow—provided insulin.  There was going to be enough for all needs.
By November 14 we were ready to share some of our experiment with the world.  Before the Journal Club of the Department of Physiology, Banting and I gave our first paper—complete with lanternslides showing blood-sugar charts.  But the crucial question we had to be answered.  Would insulin work in human beings?
Across the street in Toronto General Hospital was the 14-year old Leonard Thompson.  After two years with diabetes, he was down to 65 pounds, had scarcely the strength of lift his head from pillow.  By the usual criteria he would have, at most only a few weeks left.
We had established that insulin “cocktail” taken by mouth, did not work.  So now Banting and I rolled up our sleeves.  I injected him with our extract and he injected me—we had to be sure it wasn’t too toxic to be tolerated by human beings.  Next day we had slightly sore arms that were all.
So in January 1922, the wasted little arm of the dying boy was injected.  Testing began.  All over again, it was the story of our dogs.  Blood sugar dropped—dramatically.  Leonard began to eat normal meals.  Sunken cheeks filled out, new life came to weary muscles. Leonard was going to live! [He lived another 13 years and died in 1935—of pneumonia following a motorcycle accident].  He was the first of dozens, then hundreds, thousands, and millions to get insulin.
Honors began to shower on us.  For the best piece of research conducted at the university that year we were awarded the Reeve Prize—a welcome $50.  A grateful Parliament voted Banting a life annuity of $7500.  Then came a great research institute named for him, and later one named for me.  When Banting won the Nobel Prize in 1923 he shared the money equally with me.
Both of us stayed on at the university, and through the succeeding years concentrated on our individual research projects.  But the excitement of the old days was missing.  Then on a wintry February day in 1941, we were walking across the campus. “Charley,” said Banting, “let’s start working together again.  You handle the chemistry, and I’ll….”
It was not to be.  Three days later Banting—now a Major Sir Frederick Banting, working on problems of aviation medicine—was aboard a two-engine bomber bound for England.  The plane crashed in a snowstorm in a forest near Margraves Harbor, Newfoundland.  Banding, with a lung punctured by crushed ribs, used his waning strength to bandage the wounds of the pilot, the only survivor.  Then he lay down on pine burghs in the snow and went into the sleep from which he never awakens.
Of all eulogies, perhaps most moving was the one spoken five years at a London gathering of the Diabetics association: “without Banting this meeting could have been only a gathering of ghosts bemoaning their fate.

THE MARVELS OF HUMAN HAND

The Marvels of the Human Hand

By EVAN MCLEOD WYLIE

 Within the tightly curled, motionless organism, scarcely two inches long, millions of new cells are growing at an enormous rate.  From the side of the reck region sprouts a pair of “buds”.  Rapidly they elongate into three segments.  The extreme outer segment assumes a paddle shape.  Five lobes appear on the edges of the paddle.  Muscles, tendons and nerve fibers develop.  By the third month of pregnancy, the little flipper’s miniature fingers flex spasmodically.  A human hand has been formed.
Months later, when the baby is delivered, these little fingers will clutch and pluck at the hands of the obstetrician with startling insistence.  From then on, the hands of this human being, directed by the brain, will chiefly determine how this life differs from the lives of all other creatures on earth.
No other part of the body is so intimately associated with human behavior.  With our hands we work, play, love, heal, learn, cIn the darkness of a mother’s womb a tiny, ivory-colored embryo enters its fourth week of life. ommunicate, express our feelings, construct our civilizations and create our works of art.  The hand and our emotions are so linked that, for most of the world’s peoples, clasped hands symbolize faith, love and friendship, while the clenched fist is the unmistakable expression of human strength and resolution.
How and when during the immense span of evolutionary time did this extraordinary appendage originate?
Amazingly, the fin of the fish is the forerunner of the human hand.  As fish crept out of the sea and developed into air breathing amphibians, their fore fins developed into instruments for crawling, gripping, creeping; and through millions of years subsequent evolution their basic four-limbed artichetecture persisted.  Watch goldfish in an aquarium.  The delicate motion of the fins just behind its head as they fan the water to regulate its movements is controlled by a set of muscles, which are the rudiments of our intrinsic hand muscles.
Once of the most complex instruments of the entire body, the hand is an intricately engineered mechanical device composed of muscle, fat, ligament, tendon, bone and highly sensitive nerve fibers.  It is capable of performing thousands of jobs with precision.  To make the simplest grasping motion, and array of muscles, joints and tendons all the way from shoulder to fingertips is brought into play.  Taking a spoonful of soup involves more than 30 joints and 50 muscles.
The hand is packed full of bones, eight in the wrist, five in the palm, and 14 in the fingers of one hand.  The ligaments, cords of stringy material, hold all these bones together at the joints.  The tendons, tough fibers that guide hand and wrist bones and link them to the muscles that operate them, control finger motion.
The thumb, operating independently of the other four fingers, is the busiest and most important of all the drifts.  Because of the thumb’s unique ability to cross over and link up with any one of the other fingers, we can get along with one thumb and one other finger, or even the stump of a finger.
The rest of the fingers are markedly different in strength.  The middle finger is usually the strongest, followed by the index finger; the fourth finger is considered by the teachers of music and typewriting to be the less least responsive to training because of an innate muscular weakness; the little finger is weakest of all.
The size of a person’s hand is not significantly related to the strength of its grip or whether it will be fast or slow, deft of clumps.  Among musicians, physicians, artists, athletes and others who depend on their hands to earn living, there is an infinitive variety of stubby fingers, slender fingers, large hands and small hands.
Human fingers can be trained to perform astonishing feats.  The flying fingers of a master pianist can strike 120 notes per second.  With two fingers, a skilled surgeon can tie strands of thread into tight knots inside the human heart.  A circus performer so strengthened the index finger of his right hand by years of patient effort that he can balance himself on its tip.
Every walking moment we obtain a great deal of information about the things we touch by the “feel” of them.  This is possible because the skin of the hand is not like the skin of an other part of the body.  While extraordinary tough, it is also wonderfully elastic and incredibly sensitive.
The skin of the back of your hand actually stretches by almost half an inch when you grip or squeeze something; simultaneously, the palm inside is shortened by half and inch.  Beneath the thick skin of the palm is a buffer of fat which protects the vital tendons and blood vessels of the hand while the outer surface is being subjected to the tremendous friction created by scraping, twisting, gripping and clenching motions.
The palm of the hands, and particularly the fingertips, are equipped with special sensory apparatus.  A piece of finger skin smaller than a postage stamp contains several million nerve cells.  Of the surface of the skin are ridges formed by papillae.  These are dotted with myriad pores and nerve endings, which detect the temperature and texture of anything we touch. [Fingerprint identification is based on the fact that the whorl patterns created by these papillae are never identical in two people]
The greatest natural enemy of the human hand is cold, because bloodless joints in which the temperature drops more quickly than it does in blood filled muscles take up most of the finger.  That is why you can skate of ski all day in zero temperature without covering your face, which is full of muscles richly supplied by warm blood, while without gloves your fingers grow painfully numb in minutes.  Finger joints, like all other body joints, are bathed in a colorless, viscous lubricating fluid [synovia], which provides a smooth, gliding action when we bend an elbow or a finger.  When this fluid gets cold, it thickens and finger joints stiffen.
Because of its intricate arrangement of nerves and muscles, the hand is highly vulnerable to injury.  Injuries to wrist, fingers and hands account for almost one half of the total casualties in industrial accidents.  All lacerations of the hand are potentially dangerous because holders of virulent organisms swam over the things we touch daily.  The thick skin of the hand provides an impregnable barrier to these bacteria.  But if a scratch of puncture permits then to gain entrance, infection may follow swiftly.
Our hands deserve careful treatment.  As tools of learning, working and communicating, they can be considered the fundamental vehicle of human thought—partner with the brain in forever separating man from the rest of the animal kingdom.
tance that blocks its own 

THE WORLD'S BEST DOCTOR


“The World’s Best Doctor”

William Osler discovered no miraculous cure of wonder drug.  Yet at his death in 1919 he was the most beloved physician since Luke.  And 30 years later an article in the Journal of the American Medical Association said: “The years have added to his glory.  No one has in any way taken his place as the world’s best doctor.”
Diagnostic wizardry, brilliant research, writing and teaching—these constituted Olser’s tangible achievements.  The revolutionary methods he brought to medical schools have probably saved as many lives as the conquest of typhoid.  He was great not alone for what he did, however, but for what he was he was master of the art of ministering to a patient’s troubled mind as well as to his sick body.
William Osler (the first syllable rhymes with dose) was born in and Ontario (Canada) parsonage in 1849, the last of eight children of the Reverend Featherstone Osler.  At 15 he was expelled from the village school for unscrewing the desks from the floor one night and piling them into an attic.  Transferred to a private boarding school, he came under the influence of two remarkable men: the school warder, W.A.Johnson, and Anglican clergyman who studied natural science as a hobby; and the school physician, Dr. James Bovell, a medical man who late in life entered the ministry.  The examples of these men provided the two main streams of influence in Osler’s life: unswerving devotion to science and profound religious faith.
Few medical schools of the time owned a microscope, but Dr.Bovell did.  He and Dr. Johnson trained the eager young Osler in its use.  Shortly after he entered divinity school to study articles on microscopic fresh-water animals.  A year later he told his disappointed father that he had decided to become a doctor.
Graduating from McGill Medical School, in Montreal, Osler went to Germany, Austria and England for further study of regular clumps, which form in blood after it is drawn from the body.  Others had noticed the clumping, but Osler was the first to observe that in circulating blood there were colorless globes clumped after exposure to air, he concluded accurately that the bodies (now known as blood platelets) played an important role in clotting.  Announcement of this significant scientific discovery brought him so much acclaim that McGill called him home to become, at 24, professor of physiology.
The “boy professor” immediately converted a cloakroom into a laboratory, McGill’s first.  Then he spent $600, half of his annual income, to buy a dozen microscopes for his students.  Without appearing in the least rushed, he took on innumerable extra jobs, including those of librarian and registrar of the medical school.  New medical journals and societies seemed to sprout in his path; he probably founded more of both, and attended more meetings, than any other doctor in history.
Trichinosis was considered a rare disease in Canada—there were then only four cases on record.  But from his boyhood examination of farm animals’ viscera under the microscope Osler knew that the trichina worm turned up more often than his elders suspected and was probably sapping the strength of countless Canadians.  Now, with his own laboratory, the young professor decided to attack trichinosis; he volunteered to perform autopsies for any doctor who would let him.  Soon he was averaging 100 post-mortems a year.
Infected pork had been found to be the source of trichinosis in Europe, so for eight months Osler and a student veterinarian, A.W.Clements, haunted Montreal’s slaughterhouses, performed more than a thousand autopsies on hogs.  Finding dozens infected, they demanded that municipal meat inspection be instituted and that the public be educated to cook pork thoroughly.  This was the first of many campaigns, which were to make Osler the m most effective public-health crusader of his time.
Though his autopsies young Osler was acquiring a training in pathology that few practicing physicians could match.  He reasoned, however, that he could accomplish more if, in addition to studying the organs of those who died, he could study living patients and link their outward symptoms with an abnormal condition of some one internal organ.  But living patients were hard to come by; McGill considered young Dr. Osler purely a laboratory man and would hot permit him to examine patients in the wards of the affiliated hospital.
Several all-too reluctant physicians were then supervising the smallpox ward of the hospital on a rotating basis.  Osler volunteered to take charge of it—and thus got his first opportunity to work with sick people.  (He also got smallpox—a mild case, fortunately.)  Soon he talked his superiors into giving him a charge of a noncontiguous ward as well.
Hospitals were expected to be gloomy buildings in those days.  Osler changed all that.  He began by ordering flowers and a coat of pastel paint for the wards.  Then he went to work on his patients.  He gave them little medicine but “lavish doses of optimism,” practicing psychosomatic medicine long before the term was invented.  “The miracles at Lourdes and Ste.Anne de Beaupre,” he once wrote, “are often genuine.  We physicians use the same power every day.  It will not raise the dead; it will not put in a new eye or knit a bone; but the healing power of belief has great value when carefully applied in suitable cases.”
“To the astonishment of everyone,” recalls a Montreal doctor, “the chronic beds at McGill, instead of being emptied by disaster, were emptied rapidly through recovery, and new cases stayed but short time.  It was one of the most forceful lessons in treatment ever demonstrated.
Innovations like these spread Osler’s reputation beyond Canada and he was offered a medical professorship at the University of Pennsylvania.  Undecided, he flipped a coin; it fell “heads” for Philadelphia.  Thus, casually, American medicine was set on the road to its present excellence.
Osler’s students at Pennsylvania hardly knew what to bake of this medium-sized, athlete-looking Canadian with receding black hair, a big drooping mustache and a taste for brilliant neckties.  Instead of mounting a lecture platform, as was the professorial practice, he hitched himself up on a handy table, confessed that he hated to prepare lectures and announced that he couldn’t teach without a patient for a text anyway.  “To study the phenomena of disease without books is to sail an uncharted sea,” he stated; “but to study books without patients is not to go to sea at all.”
Accordingly, he introduced a thin young man and told the class to see for themselves what a real live case of anemia looked like.  Patients illustrating other diseases followed, all lucidly analyzed by Osler.  The medical students were electrified; it was the first time most of them had ever tapped a patient’s chest, listened to a heartbeat of examined blood under a microscope.  For at that time [18840 no medical school in the United States offered effective “on-the-job” beside teaching.  ‘It makes one’s blood boil,” Osler fumed, ‘to think that there are sent out year by year scores of men called doctors who have never attended a case of labor or seen the inside of a hospital ward.”
Not content with bringing patients to his students, Osler now brought students to patients.  For the first time anywhere, medical students entered hospital wards freely, as much a part of the team as interns, nurses or attending physicians.  They took case histories, examined patients [under close supervision, of course] and made tentative diagnoses that were confirmed or corrected by the experienced doctor in charge.
As Osler hade predicated, the patients received better, more alert care than ever before, with fewer mistakes, thanks to the constant stimulus of inquiring young minds for who diagnoses had to be checked and counterchecked.  The cornerstone of all medical education today, William Osler’s bedside teaching pays dividends in better medical care to every human being now alive.
In Baltimore the trustees of the will of a merchant prince named Johns Hopkins were now building the finest hospital and medical school in the continent.  Searching Europe and America for physician-teachers, they chose William H Welch to head their pathology department; Howard Kelly, gynecology; William Stewart Halsted, surgery; and William Osler, internal medicine.  Of Johns Hopkins’ famed “Big Four,” the oldest, Osler, had not yet reached his 40th birthday.
From the day it opened in 1889, brilliant youngsters flocked to the new Baltimore center, and within a few years Osler’s trainees in particular were eagerly sought from New York to San Francisco.
Dr. Osler’s ward rounds, starting promptly at 9 a.m., were the high spot of the hospital day.  Nurses, interns and visiting doctors made an admiring procession in his wake.  Patients knew (they were supposed to know) a great man was coming to help them, and they smiled.  For his children, to whom he was particularly devoted, he had a “secret” whistle, a prearranged signal to warn them of his approach.
Osler was an uncanny diagnostician, a bedside sleuth with few equals.  He knew what to look for, and he took the time to find it.  In one patient, for example, he suspected the presence of an arterial aneurysm—a dangerously dilated blood-vessel sac that, if it could be located, might be removed surgically.  If not, it might hemorrhage fatally.  Repeated physical examinations had failed to turn up the elusive sac when Osler appeared at the bedside.
For an hour, while interns grew restless, the Chief just sat there watching the sick man’s chest and abdomen.  Finally he said, “let’s try swinging the bed around to the far wall.”  Puzzled, the interns complied.
Lifting the window shaded high, Osler studied his patient only a moment in the new light, and then pointed on the chest wall.  There, faintly but unmistakably shadowed by the slanting afternoon sunshine, was the telltale pulsation of the aneurysm none else had been able to find.
Often Osler could diagnose quickly.  Leading his students through a ward one morning, he passed the bed of a patient whom he had ever seen before.  Grasping the man’s toes for an instant he waved good-bye, and as soon as they were out of earshot he informed his startled retinue that the owner of the tows suffered form leakage of a heart valve.  No undergraduate who saw him pull that diagnostic rabbit out of the hat ever forgot that this particular heart condition causes a distinctive jerky pulse, easily observed in the big toe.
Among the visiting doctors who followed Osler through the wards one day was an unknown young country surgeon from Minnesota.  Osler’s through study of patients and the constant use of scientific diagnostic aids like the microscope made a deep impression on him, and he came back many times with his brother.  The brothers’ name was Mayo.
Another young man used to wander over from the surgical department to watch Osler—a young man so impatiently outspoken about the work of other staff surgeons that rumor said his days at Johns Hopkins were numbered.  Sensing his potential greatness, Osler gently suggested self-restraint.  The hotheaded young man offered to resign.  Next morning he had a note for Osler.  “Do nothing of the kind!” it said.  “Who is free for faults?  Your prospects here are A-1 and we need you.”  So it was that Harvey Cushing stayed at John Hopkins to blaze new trials in brain surgery and to become William Osler’s devoted son in all but name.
Duties at Johns Hopkins were just part of Dr. Osler’s activities.  He was also president of the American Pediatric Society, author of a neurological study of cerebral palsy, an authority on angina pectoris and certain other circulatory aliments (on is still called Osler’s disease), co-founder of the National Tuberculosis Association, of Christmas Seal fame.  He was a crusader against malaria, typhoid and syphilis, and a pioneer advocate of better mental hospitals.  Meanwhile, he wrote no less than 1200 books and articles, an amazing average of one every two weeks during his adult life.  Some of them remain classic in their field, unexcelled even after a half century of medical advance.
In 1897 a Baptist minister in Montclair, New Jersey, read Osler’s ‘Principles and Practice of Medicine’ and was both enthralled and appalled.  In it Osler had summed up all that medical science knew at that time, then bluntly declared there was much more it should know and didn’t.  The minister was Frederick Gates, philanthropic adviser to John D. Rockefeller, Sr. He discussed Osler’s book with Rockefeller, and out of that conference grew the Rockefeller Institute for Medical Research and, later, the Rockefeller Foundation.
By 1905 Osler, besieged by sick people, working at a killing pace, concluded that if he were to retain his own health he would have to find a quieter post than John Hopkins.  Medical schools all over America sought him; a Canadian millionaire offered McGill $1,000,000 if it could get him back.  But his choice was made when King of England appointed him Regis Professor of Medicine at Oxford.  A few years later the King conferred on him the baronetcy that made him Sir William.
His first move in England was to make peace between London’s two rival medical societies, which had not spoken to each other for 50 years.  His second was to reintroduce bedside teaching to a nation, which had neglected its potentialities.  Osler took Britain to his heart, and she took hi to hers.  His Oxford home became a sort of New World embassy in the Old, fabulous for its hospitality.
Too old for front-line duty in World War 1, Osler went into uniform as a medical consultant to the Canadian and American Army hospitals in England, and unofficially earned the title of Army Consoler General.”  He received hundreds of anxious cables for next token whose wounded soldiers were hospitalized in Britain.  In each case he located and examined the wounded man.  The Canadian Medical Corps adopted for parents the most reassuring from cable it could think of: “Your son has been seen by Osler and is doing well.”
In August 1917 Sir William’s own son and only child, 21-year-old Revere Osler, was gravely wounded at Ypres.  Half a dozen of the American Army’s greatest surgeons—Harvey Cushing and George Crile among them—sped to the scene.  An operation was performed, but in vein.  With heavy hearts they watched as the Chief’s beloved boy was lowered into the earth of Flanders.
Following the Armistice, Sir William spent a year raising money to save the war-ravaged libraries of Allied Belgium and the starving children of ‘enemy’ Austria.  Then, in December 1919, worn oust by his wartime activities and by grief for his son, he was unable to withstand an attack of pheneumonia that followed recurrent attacks of bronchitis.  Knowing more about the disease than his attending physicians, he realized how it would end for him, and faced death serenely.
After he died a slip of paper found on his bed.  On it he had written: “The Harbor almost reached after a splendid voyage, with such companions all the way, and my boy awaiting me.”